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Expression data from H9 human embryonic stem cells (hESCs) infected with either lentiviral non-silencing shRNA or shRUNX1, and differentiated to early mesendoderm

ABSTRACT: We used microarrays to detail the global program of gene expression during early hESC differentiation to mesendoderm using FBS, with and without RUNX1 depletion.

ORGANISM(S): Homo sapiens

PROVIDER: GSE79598 | GEO | 2016/10/06

SECONDARY ACCESSION(S): PRJNA316339

REPOSITORIES: GEO

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Expression data from H9 human embryonic stem cells (hESCs) differentiated to Early Mesoendoderm

Project description:We used microarrays to detail the global programme of gene expression during early hESC differentiation to Mesendoderm using FBS.

2016-03-22 | GSE74004 | GEO

Expression data from H9 human embryonic stem cells (hESCs) differentiated to Early Mesoendoderm

Project description:We used microarrays to detail the global programme of gene expression during early hESC differentiation to Mesendoderm using FBS. Samples of hESCs were taken at undifferentiated state (0h), 8h of differentiation, 24h of differentiation, and 72h of differentiation with three replicates (A, B, and C) at each time point.

2016-03-22 | E-GEOD-74004 | biostudies-arrayexpress

Mesendoderm induction

Project description:ES cells are differentiated into mesenderm cell linage by Activin A treatment. During this differentaition, gene expression profile of ES cells, day 4 mesendoderm cell, day 5 mesendoderm cells and mesoderm cells are examined.

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Genome-wide profile of 5-hydroxymethylcytosine (5-hmC) in H9 human embryonic stem cells (hESCs)

Project description:The link between single cell variation and population level fate choices lacks an explanation despite extensive observations of gene expression and epigenetic variation among individual cells. Here, we found that single human embryonic stem cells (hESCs) have different and biased differentiation potentials toward either neuroectoderm or mesendoderm depending on their G1 lengths before the onset of differentiation. Single cell variation in G1 length establishes a probability distribution in which increased variation biases stem cells toward neuroectoderm. Although sister stem cells generally share G1 lengths, a variable proportion of cells have asymmetric G1 lengths, which maintains the population dispersion. WNT levels control the G1 length distribution apparently as a means of priming the fate of hESC populations once they undergo differentiation. Global 5-hydroxymethylcytosine levels are regulated by G1 length and thereby link G1 length to differentiation outcomes of hESCs. Our findings suggest G1 length distribution links intra-population heterogeneity to population outcome.

2019-01-01 | GSE113236 | GEO

Expression data from human embryonic stem cells (hESCs) and Activin-induced/derived cells

2011-05-21 | GSE29421 | GEO

RNA-seq of retinal organoids differentiated from hESCs carrying mutations in the RB1 gene

Project description:hESC lines carrying deleterious mutations in the RB1 gene in heterozygous and homozygous state were generated by genome-editing based on CRISPR/Cas9. Parental cell line and genome-edited cell lines were differentiated into retinal organoids for 152 days based on the Protocol published by Döpper et al., Current protocols, PMID: 32956559. Briefly, single cells were reaggregated in presence of dual SMAD and WNT-inhibition; retinal tissue became visible from day 12 onward. BMP4-induction and addition of small molecules CHIR99021 and SU5402 directed differentiation towards retina and retinal pigment epithelium. Long-term differentiation was carried out in the presence of 10% FBS, taurine and retinoic acids. Organoids were collected at indicated time points and either embedded for cryosectioning and immunostaining or frozen at -80°C for RNA preparation.

2022-05-10 | E-MTAB-10331 | biostudies-arrayexpress

p53 coordinates Wnt and TGF-β inputs on mesendoderm differentiation genes

Project description:The TGF-β superfamily member Nodal triggers mesendoderm differentiation in embryonic stem (ES) cells. This transition however requires cooperating Wnt signaling inputs. Here we report that p53, a powerful tumor suppressor in adult tissues, orchestrates this cooperation. We show that p53, which is released from inhibition as mouse ES cells exit from pluripotency, acts as a direct inducer of Wnt3 expression. Wnt-activated Tcf3 then converges with Nodal-activated Smad transcriptional complexes on mesendoderm specification super-enhancers. p53 and its homolog p73 act redundantly in Wnt induction. When p53 and p73 are depleted, the ES cells fail to secrete autocrine Wnt ligands, Tcf and Nodal-activated Smads fail to bind to mesendoderm gene enhancers, and the cells adopt ectoderm rather than mesendoderm identity. Enforced Wnt3 expression or addition of Wnt3a rescues mesendoderm differentiation in p53/p73-depleted ES cells. Thus, independently of their established role as tumor suppressors that guard genome integrity in mature cells, p53 and p73 serve a primordial role in ES cell differentiation by driving a cooperation of Wnt and TGF-β transcriptional inputs on mesendoderm identity gene enhancers.

2017-01-06 | GSE70486 | GEO

ChIP-seq of FOXK2 in human embryonic stem cells H1 ESC, and the differentiated mesendoderm cells and and NPC cells

Project description:In order to investigate the genome-wide binding profile of the forkhead transcription factor FOXK2 in human embryonic stem cells (ESCs) and downstream cell types, we generated the ChIP-seq data of FOXK2 in H1 ESC cells and two differentiated types of cells, mesendoderm cells and NPC cells.

2020-12-21 | E-MTAB-9630 | biostudies-arrayexpress

Expression data from human embryonic stem cells (hESCs) and Activin-induced/derived cells

Project description:Nodal/Activin signaling directs mesendoderm specification in early vertebrate embryogenesis. We have characterized transcriptional profiling of human embryonic stem cells and Activin-treated cells at different timepoints. In this dataset, we include the timecourse gene expression data obtained from hESC differentiation post Activin treatment, examining at day 0, 1, 3 and 5. Four biological replicates were used for day 0, three for day 1, three for day 3, and four for day 5. Cells were harvested and used for total RNA preparation using Trizol (Invitrogen). Gene expression was analyzed using GeneChip Human Exon 1.0 ST Array (Affymetrix).

2011-05-21 | E-GEOD-29421 | biostudies-arrayexpress

Comparison non-targeting hRNA hESCs versus UBE2K shRNA hESCs

Project description:Histones modulate gene expression by chromatin compaction, regulating numerous processes such as differentiation. However, the mechanisms underlying histone degradation remain elusive. When compared with their differentiated counterparts, immortal human embryonic stem cells (hESCs) have a unique chromatin architecture and low levels of trimethylated histone H3 at lysine 9 (H3K9me3), a heterochromatin-associated modification. Here we assess a link between the intrinsic epigenetic landscape and ubiquitin-proteasome system of hESCs. We find that hESCs exhibit high expression of UBE2K, a ubiquitin-conjugating enzyme. Loss of UBE2K increases the levels of H3K9 trimethyltransferase SETDB1, resulting in H3K9 trimethylation and repression of neurogenic genes during differentiation. Concomitantly, loss of UBE2K impairs the ability of hESCs to differentiate into neural progenitors with neurogenic properties. Besides H3K9 trimethylation, we find that UBE2K binds histone H3 to induce its polyubiquitination and degradation by the proteasome. Notably, ubc-20, the worm orthologue of UBE2K, also regulates both histone H3 levels and H3K9 trimethylation in C. elegans germline. Thus, our results indicate that UBE2K crosses evolutionary boundaries to promote histone H3 degradation and reduce H3K9me3 repressive marks in immortal cells.

2020-06-01 | PXD018625 | Pride

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